Um, what evidence would be needed to determine whether it is microplastics that contribute to inflammation or fibrosis rather than just simply accumulating in a tissue that has already undergone al- alterations?

Of course, both possibilities can be conceived.

It is possible that, uh, microplastics and nanoplastics promote inflammation and fibrosis, but as you said, it is also possible that, uh, a preexisting inflammatory situation, inflammatory environment with a burden, a higher burden of macrophages is more likely to uptake microplasti- mi- microplastic because, uh, macrophages have, have, um, very high phagocytic activity.

We already have a number of, uh, preclinical molecular in vitro studies suggesting, uh, the possibility that microplastics, uh, consistently promote inflammation and fibrosis.

Some of these studies are of good quality, some others are not because mainly, uh, most of the in vitro studies were performed with very high doses of microplastics, unlikely to be realistic or relevant or pertinent for human exposure.

And also, most of them were done with the only one type of plastic.

The most studied plastic was polystyrene, which is not the only one we found.

There's a lot of, uh, causation mechanisms that m- still need to be established, but do we need to prioritize any measures for reducing plastic emissions and, uh, improving monitoring in high-risk populations? And is there any practical advice that can be given to populations facing high exposures?